The article differs substantively from the actual conclusions of the study. This study shows a minor correlation in some bacterial DNA "signatures" in arterial plaque in about 200 people (~40% had the correlated bacteria). The study only included tissues from people who died of heart disease or had surgery related to heart disease. There does not currently appear to be a strong baseline about how widespread this bacterial signature may exist in a broad population regardless of health.
In a nutshell there is a slightly interesting idea that deserves further study. That's it.
So, one could make a similar article saying "Myocardial infarction may be caused by sugar consumption" and support it by analyzing the recent diet of 200 people who died of heart disease and finding that 95% of them recently consumed a lot of sugar.
I might be reading parts of it wrong, but I think that's a different sort of thing to the research in the article.
Sugar is a very indirect cause of heart attacks, everyone knows that most heart attacks are a culmination of decades of diet and exercise habits. It's still worth researching everything to do with that, but it's pretty low value research because it's hard to draw any actionable conclusions from it other than "eat healthier and exercise", which is already well known.
The research in the article is talking about a direct cause. Bacteria exists on arterial plaque, viral infection triggers bacteria to multiply, something about that process causes the plaque to detach and cause a heart attack. If that ends up being a rock solid cause and effect, even for a subset of heart attacks, that could lead to things like direct prevention (anti-virals before the heart attack happens) or changes in patient management (everyone with artery disease gets put far away from sick patients) that could directly and immediately save a lot of lives.
The post you replied to was saying that the data from the study isn't as strong as the article and headline make it out to be, which is usually the case. For this one though I'm reading that less as "it's a nothingburger" and more as "it's a small interesting result that needs a lot of follow up".
Isn’t it obvious that a heart attack could be caused by a myriad of issues? Sure a bacteria could be a cause. So could be genetics, or an excess of cheeseburgers. A heart ceasing to pump blood effectively is not a singular cause
Minor correlation? P values are small indicating a strong correlation?
Quote: Of the bacteria detected, oral viridans group streptococcal DNA was the most common, being found in 42.1% of coronary plaques and 42.9% of endarterectomies. Immunopositivity for viridans streptococci correlated with severe atherosclerosis (P<0.0001) in both series and death from coronary heart disease (P=0.021) or myocardial infarction (P=0.042).
This is a super common misconception, but a small p-value does *not* (necessarily) mean a strong correlation. It means high confidence that the correlation is non-zero.
•
Could a short‐term antibiotics treatment given at the acute phase affect the outcome of myocardial infarction, and would it be possible to develop new diagnostic imaging and prevention methods for bacterial biofilm?
I think the first question to be addressed should be, does the general population have similar prevalence of this bacteria?
I didn't read the article but just based on the parent comment, it sounds like this baseline hasn't yet been established. It seems very wrong to start testing antibiotics without first establishing the baseline of whether everyone has this bacteria.
It's not even "here's another way this can happen" - there's no real evidence that the bacteria are causing the heart disease. Just a fact that 40% of the 200 people with the heart disease had the bacteria, and no baseline for whether everyone else normally has those bacteria.
Of course it depends on fractions. You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection. So knowing that all the plans towards eliminating this disease focus on HPV.
On the other hand most people with "flu" in summer months are not infected with Influenza, so an improved influenza treatment isn't going to make a big difference for them unlike in winter. We know other reasons you might get those symptoms which are more likely in summer.
Peptic ulcers are another well-known case, in which most (though not all) instances can be traced to a Helicobacter pylori infection. Other causal factors include NSAID usage, stress, and diet.
One of the rare examples of a mental health condition being virtually completely eliminated is that of General paresis of the insane, a symptom of late-stage syphilis.
Successful treatment and elimination of syphilis in patients and populations through antibiotics. As one of the few cases of near-total elimination of a class of mental conditions, this a useful reminder to the psychiatric profession that not all mental conditions have causes limited to the brain and its function, whether through its biochemistry or neural/behavioural processes.
> You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection.
What are these other ways? There's an intuition that bodies are like computer programs that can fail in unpredictable ways, but this is usually false and belies a failure to see links between 'novel' and previously described mechanisms.
Anecdotally, I had a myocardial infarction at 23, and I was honestly surprised to learn that it wasn’t already well known that infectious diseases could trigger such events.
Up until that point, I’d never had any heart-related issues, nor does anyone in my family. Just two days before being admitted to the hospital with a suspected heart attack, I came down with food poisoning. It wasn’t pleasant, of course, but I thought it was nothing unusual—something a couple of days of rest and hydration would normally resolve.
Since my bloodwork at the hospital matched the expected results for a heart attack, and I underwent surgery, the doctors understandably focused on treating the immediate problem rather than identifying the underlying cause (I’m eternally grateful to the team and staff at St. Vincentius-Kliniken. I truly don’t think I’d be here without them).
That said, I’m glad to see this area receiving more attention. Hopefully, it will lead to further studies and the development of better strategies for prevention and treatment.
Can you clarify -- if you're comfortable sharing additional details -- did you have an "occlusion MI" heart attack, involving balloons / stents in the cath lab?
Most people assume that "heart attack" is a distinct clinical entity, but the majority (~80%) of elevated troponin levels are not exactly what comes to mind when people say "heart attack," but will often be described to patients as a heart attack (sometimes out of ignorance and others out of convenience, as the actual explanation for what is going on takes a lot more time and effort).
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix…”
Phages can penetrate biofilms [1]. (They have practice.)
There are countless ways to make medicines and treatments around old technologies and other things that are off-patent, in a way that is novel and able to be patented.
Even boring old generic medicines often find themselves reformulated into new treatments as combinations, variations, or in some cases simply a different dose and indication.
Phages are intensely species specific to bacterial species, so they don't work unless you identify exactly what you're targeting. Also, even if they can penetrate biofilms, that doesn't mean you can successfully deliver them to the biofilm in the human body, since they have to survive the whole blood stream and the normal human immune response to "not self" things.
> you can't patent phages, so we'll just continue ignoring them
Nope. Plenty of governments fund this sort of research. And chances are there isn’t an off-the-shelf phage that ticks the boxes, which means you need some amount of genetic engineering, in which case Monsanto has your back.
This is a nicely-designed study. For decades, we've known that inflammation is a risk factor for heart attacks.
In this study, the researchers designed a custom antibody that binds to oral bacteria. Then they used histological staining to identify specific biofilm structures inside the atherosclerotic tissue. Bacteria released from the biofilm were observed in heart attack cases, which gives us evidence that when the body's immune system responded to these bacteria, it triggered inflammation which ruptured cholesterol-laden plaque. So now we have more insight into the mechanism behind why inflammation is associated with heart attack risk.
The "pantheon" of risk factors for heart disease are:
* hs-CRP (inflammation): the mechanism studied by this research. High inflammation roughly doubles your risk of heart disease.
* ApoB - 20% of people with normal cholesterol will have abnormal ApoB, and be at risk of heart disease (ApoB is a structural protein in lipoproteins which cause arterial plaque).
* Lp(a) - the strongest hereditary risk factor for heart disease (Lp(a) acts as a multiplier on ApoB, since it camouflages cholesterol particles from your liver)
* HbA1c - insulin resistance /diabetes is a risk factor for just about everything.
* eGFR - estimates the volume of liquid your kidneys can filter, and is an input to the latest heart disease risk models (PREVENT).
You should probably disclose that the order link at the end of your post goes to your own company.
Basic LDL cholesterol and triglycerides blood panels are still an essential part of heart disease bloodwork, too.
I would suggest most people start by asking your doctor for some of these tests at your next annual checkup, as many of them and the doctor visit are likely covered by insurance. The ACA has special handling for routine annual checkups, so don’t assume it’s going to be expensive until you’ve checked the cost with your insurance. A routine bloodwork panel will also include a number of other important measures that are routine and very cheap. It’s helpful to have all of these on your medical record so trends can be identified over time.
Basic LDL cholesterol is often covered by insurance, but ApoB, Lp(a), and hs-CRP are unfortunately usually not. If insurance doesn't end up covering it, sometimes the fee is just ridiculous.
Part of why we do cash pay (and pre-negotiated pricing with the labs) is that you avoid weird catastrophic scenarios like this. The price is upfront and transparent.
(It's too late to edit the original post, but my affiliation is on my HN profile.)
1) Isn't ApoB measurement pretty much in tandem with LDL, VLDL, and triglycerides? I realize it's being recognized now as the necessary factor for arterial dysfunction, but it seems like a lot of hoopla is being made as if it were some "silent" overlooked factor when for the vast, vast majority of people their ApoB levels are entirely explained by the other 3 lipid panel line items carrying it, and they have been in use for decades and are strongly targeted by the medical establishment
2) Isn't Lp(a) a separate lipoprotein altogether which is an independent risk factor for MACE? I've never heard of it "disguising" other cholesterol in testing.
1) ApoB itself is more accurate than LDL and triglycerides. The latest evidence is that ApoB and Lp(a) together are more accurate than even LDL, VLDL, non-HDL, triglerycerides, etc combined: https://academic.oup.com/eurheartj/article-abstract/46/27/27...
2) The terminology is confusing, but each Lp(a) particle is "just" a cholesterol particle wrapped with an extra protein, apoprotein (a). So each Lp(a) particle includes one ApoB molecule (the structural protein in atherogenic cholesterol particles) and many cholesterol and triglyceride molecules, but the extra protein makes each Lp(a) particle about 6x more atherogenic than a typical cholesterol particle.
there's a small subset of people with more atherogenic triglycerides that ApoB picks up over and above just tracking with the LDL, but...you probably knew that just looking at them
The standard risk model based on SCORE-2 and PREVENT like parameters are very poor as reported in the recently published paper on the their accuracy performance by the Swedish team [1].
>All of these risk factors can be measured with a blood test + doctor review
As all CVD risk stratification with cardiologist review, the most important accuracy is sensivity (avoiding false negative that will escape review) of SCORE-2 and PREVENT, 48% and 26%, respectively [1].
The paper alternative proposal increased the sensitivity to 58% by performing clustering instead of conventional regression models as practiced in the standard SCORE-2 (Europe) and PREVENT (US).
These type of models including the latest proposal performed very poorly as indicated by their otherwise excellent and intuitive display of graphical abstract results [1].
[1] Risk stratification for cardiovascular disease: a comparative analysis of cluster analysis and traditional prediction models:
For lipids, besides the named tests, HDL, LDL, and triglyceride tests are older but shouldn't be overlooked.
For measuring inflammation, besides hs-CRP, additional tests are relevant and overlooked: regular CRP, ESR, and homocysteine.
Additionally, a heart attack can result from parasite induced inflammation too, e.g. in chagas disease, which is becoming increasingly common in the US while being very undetected without explicit testing. It is also very difficult to treat, but the gist 4196f31d12a43a95756e792500ff516f has some info on treating it. Lyme disease too can harm the heart permanently. In both cases a pacemaker could help as applicable.
Can you expand more on why you'd want regular CRP over hs-CRP (specifically for cardiovascular risk)?
For homocysteine, one proxy is B12 or folate (which are more cost-effective to test). To my knowledge, ESR is used in certain rheumatologic conditions, and was used more often in the past, but isn't currently used for heart disease.
Yeah. If you don't have obvious symptoms, they'd likely prescribe you a statin, metformin, or some sort of dietary intervention. But you'd want to discuss it with your doctor in any case...
This particular panel includes a consult with a doctor (who can advise on next steps, prescribe medication, and so on). Or you can take the results to your doctor.
The original title is "Myocardial infarction may be an infectious disease" which appears to be clickbait, with the title posted here being much more accurate.
Immune response to bacteria in arterial plaques can cause them to break up and cause the attack (my lay-interpretation) so the bacteria is a trigger, but "infectious disease" is a bit of hyperbole.
> bacteria in arterial plaques can cause them to break up and cause the attack
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix” whose rupture “result[s] in thrombus formation and ultimately myocardial infarction” sounds like infection more than careless bacteria kicking up muck.
Not all infarctions are due to infectious disease. The title (even on HN) is incorrect.
"Some myocardial infarctions attributed to an infectious
disease."
"A myocardial infarction may be due to infectious disease."
My maternal grandfather died of an aortic separation. This caused a myocradial infarction, which was not due to infectious disease. I had my aortic valve replaced with a mechanical when I was 2, and 9, and 31, so I'll have a more nuanced kind of heart failure.
Have always been fascinated with Paul Ewald's arguments (as laid out in his books The New Germ Theory of Disease and Evolution of Infectious Disease) that most chronic illnesses are due to pathogens.
"The most unique finding in our study was that viridans streptococci seemed to colonize the lipid core and wall of an atheroma as a biofilm and that this biofilm was not recognized by cells of the innate immune system. "
This is a pretty cool finding. Biofilms are also beyond reach of antibacterials usually. And seing a commensal become a problem due to "location, location, location" is also cool.
For the Listerine part: they are referencing this study: https://pubmed.ncbi.nlm.nih.gov/16373688/ that seems to show a correlation between poor oral health and sudden cardiac death, so it might help indeed, with other good oral health practices.
I only use very dilute Listerine - for the fluoride. A dentist told me that undiluted, alcohol based products can cause tissue damage (which conceivably would result in a vector for oral bacteria infiltrating to the bloodstream?)
I probably should find sources first but I was always under the impression that the mouth biome is strongly correlated to gut biome which strongly correlated to immune system.
TFA says the biofilms protect the bacteria from antibiotics. Better approach is probably engineered antibodies or even a phage (engineered virus that attacks the bacteria).
Yes, there are studies where they compared heart attack rates for people who'd taken a course of antibiotics with those who hadn't and there was quite a large effect in some of them.
Titles like this are very confusing. The paper better explains it, but a disease can't be contagious or infectious. The paper describes a link between a potential bacterial infection and myocardial infarctions that may take years or decades to develop.
The disease is only the named group of symptoms. The potential cause of the disease is the bacterial infection. Those are very different concepts.
Wild I see only one mention of COVID so far, it has been shown to attack all kinds of organ tissues, the perspectives around "with or from" somehow permanently prevents people from discussing the underlying changes from this continued global cycling of the pathogen.
How does flu affect the heart? The virus only rarely infects the heart directly. Instead, the adverse effects of the virus on the heart are due to atherosclerosis of the arteries of the heart. Many people over age 50 have atherosclerosis — and in some people it has not yet been diagnosed. Because atherosclerosis narrows the arteries and reduces the flow of blood, less oxygen reaches the heart muscle. When the effect of the flu on the lungs lowers the amount of oxygen in the blood, this further reduces the supply of oxygen to the heart. This can lead to a heart attack or cardiac arrest (sudden death).
Is this risk more than theoretical? Many careful studies have shown there is an increased risk of heart disease following a bout of flu. In one study of 80,000 adults with influenza, nearly 12% had a serious cardiac event, such as a heart attack, during or in the weeks after getting the flu.
> In one study of 80,000 adults with influenza, nearly 12% had a serious cardiac event, such as a heart attack, during or in the weeks after getting the flu.
That sounds really high
Okay I just looked it up and this was only among hospitalized individuals which makes a lot more sense because most people just stay home unless it's very bad but that is still surprising to me
In the context of the article, it's inflammation rupturing the 'fibrous cap' on plaque deposits leading to a heart attack, so I presume OP is talking about the inflammatory response to having the flu.
Even temporary stress on the respiratory system can cause long-term damage to the brain, lungs, and heart. Because of Covid, we started to learn that an acute, severe infection can affect people much later.
That research led to the beginning of an understanding that repeated flu infections can contribute to premature death even many decades later.
It's been known for many years that the flu vaccine reduces heart attack incidence. The flu either causes lasting damage to the cardiovascular system or directly causes heart attacks.
This is perfectly well known and absolutely nothing new.
This study merely expands research on the topic (focus on bacteria+biofilm instead of flu).
So "Myocardial infarction may be an infectious disease" is a weird clickbait title. We know. We knew for a long time.
We also have quite a few of anti biofilm agents in IV formulations that could have an effect inside of the cardiovascular system if used in high dosages, but the molecules are old, cheap and unsexy, so no one will try. (ambroxol and NAC come to mind)
Typical of the medical field: one of the most studied diseases in the past several decades and now there is a ground-breaking new study that questions all knowledge.
I blame the corruption from American medical experts and organizations which only object is to sell drugs.
This does not question all knowledge. Bacteremia and cardiac disease have been linked for years (see upvoted comment above), which is why these studies were done in the first place. This study isn't ground breaking, it's extending an already established area of study.
Furthermore, while there are issues of misaligned incentives across the industry, of the top 10 pharma companies: Roche, AstraZeneca, Bayer, Novartis, Sanofi, Novo Nordisk, GSK, are all based in Europe, so your assertion further down makes no sense.
This idea is not supported by the study in question. Even if it were, what you’re describing is just how science works! The cynicism, while understandable, seems widely irrelevant here.
The article differs substantively from the actual conclusions of the study. This study shows a minor correlation in some bacterial DNA "signatures" in arterial plaque in about 200 people (~40% had the correlated bacteria). The study only included tissues from people who died of heart disease or had surgery related to heart disease. There does not currently appear to be a strong baseline about how widespread this bacterial signature may exist in a broad population regardless of health.
In a nutshell there is a slightly interesting idea that deserves further study. That's it.
Interesting.
So, one could make a similar article saying "Myocardial infarction may be caused by sugar consumption" and support it by analyzing the recent diet of 200 people who died of heart disease and finding that 95% of them recently consumed a lot of sugar.
I might be reading parts of it wrong, but I think that's a different sort of thing to the research in the article.
Sugar is a very indirect cause of heart attacks, everyone knows that most heart attacks are a culmination of decades of diet and exercise habits. It's still worth researching everything to do with that, but it's pretty low value research because it's hard to draw any actionable conclusions from it other than "eat healthier and exercise", which is already well known.
The research in the article is talking about a direct cause. Bacteria exists on arterial plaque, viral infection triggers bacteria to multiply, something about that process causes the plaque to detach and cause a heart attack. If that ends up being a rock solid cause and effect, even for a subset of heart attacks, that could lead to things like direct prevention (anti-virals before the heart attack happens) or changes in patient management (everyone with artery disease gets put far away from sick patients) that could directly and immediately save a lot of lives.
The post you replied to was saying that the data from the study isn't as strong as the article and headline make it out to be, which is usually the case. For this one though I'm reading that less as "it's a nothingburger" and more as "it's a small interesting result that needs a lot of follow up".
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Isn’t it obvious that a heart attack could be caused by a myriad of issues? Sure a bacteria could be a cause. So could be genetics, or an excess of cheeseburgers. A heart ceasing to pump blood effectively is not a singular cause
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Minor correlation? P values are small indicating a strong correlation?
This is a super common misconception, but a small p-value does *not* (necessarily) mean a strong correlation. It means high confidence that the correlation is non-zero.
P value means "if the null hypothesis were true, the probability we would have observed what we actually observed."
It's definitely not the strength of correlation. It's not even the probability that the opposite of the null hypothesis is false!
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yes from tfa:
What Question Should Be Addressed Next?
• Could a short‐term antibiotics treatment given at the acute phase affect the outcome of myocardial infarction, and would it be possible to develop new diagnostic imaging and prevention methods for bacterial biofilm?
I think the first question to be addressed should be, does the general population have similar prevalence of this bacteria?
I didn't read the article but just based on the parent comment, it sounds like this baseline hasn't yet been established. It seems very wrong to start testing antibiotics without first establishing the baseline of whether everyone has this bacteria.
I assume this is a "here's another way this can happen" rather than "actually this is caused only by this and not by what we used to think"?
It's not even "here's another way this can happen" - there's no real evidence that the bacteria are causing the heart disease. Just a fact that 40% of the 200 people with the heart disease had the bacteria, and no baseline for whether everyone else normally has those bacteria.
Surely this? The number of ‘oh, it turned out to be more more complicated’ scenarios in medicine is high.
Of course it depends on fractions. You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection. So knowing that all the plans towards eliminating this disease focus on HPV.
On the other hand most people with "flu" in summer months are not infected with Influenza, so an improved influenza treatment isn't going to make a big difference for them unlike in winter. We know other reasons you might get those symptoms which are more likely in summer.
Peptic ulcers are another well-known case, in which most (though not all) instances can be traced to a Helicobacter pylori infection. Other causal factors include NSAID usage, stress, and diet.
<https://en.wikipedia.org/wiki/Peptic_ulcer_disease>
<https://en.wikipedia.org/wiki/Timeline_of_peptic_ulcer_disea...>
One of the rare examples of a mental health condition being virtually completely eliminated is that of General paresis of the insane, a symptom of late-stage syphilis.
Successful treatment and elimination of syphilis in patients and populations through antibiotics. As one of the few cases of near-total elimination of a class of mental conditions, this a useful reminder to the psychiatric profession that not all mental conditions have causes limited to the brain and its function, whether through its biochemistry or neural/behavioural processes.
<https://en.wikipedia.org/wiki/General_paresis_of_the_insane>
1 reply →
> You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection.
What are these other ways? There's an intuition that bodies are like computer programs that can fail in unpredictable ways, but this is usually false and belies a failure to see links between 'novel' and previously described mechanisms.
3 replies →
Anecdotally, I had a myocardial infarction at 23, and I was honestly surprised to learn that it wasn’t already well known that infectious diseases could trigger such events.
Up until that point, I’d never had any heart-related issues, nor does anyone in my family. Just two days before being admitted to the hospital with a suspected heart attack, I came down with food poisoning. It wasn’t pleasant, of course, but I thought it was nothing unusual—something a couple of days of rest and hydration would normally resolve.
Since my bloodwork at the hospital matched the expected results for a heart attack, and I underwent surgery, the doctors understandably focused on treating the immediate problem rather than identifying the underlying cause (I’m eternally grateful to the team and staff at St. Vincentius-Kliniken. I truly don’t think I’d be here without them).
That said, I’m glad to see this area receiving more attention. Hopefully, it will lead to further studies and the development of better strategies for prevention and treatment.
Can you clarify -- if you're comfortable sharing additional details -- did you have an "occlusion MI" heart attack, involving balloons / stents in the cath lab?
Most people assume that "heart attack" is a distinct clinical entity, but the majority (~80%) of elevated troponin levels are not exactly what comes to mind when people say "heart attack," but will often be described to patients as a heart attack (sometimes out of ignorance and others out of convenience, as the actual explanation for what is going on takes a lot more time and effort).
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix…”
Phages can penetrate biofilms [1]. (They have practice.)
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC8875263/
But you can't patent phages, so we'll just continue ignoring them
This is basically a myth.
There are countless ways to make medicines and treatments around old technologies and other things that are off-patent, in a way that is novel and able to be patented.
Even boring old generic medicines often find themselves reformulated into new treatments as combinations, variations, or in some cases simply a different dose and indication.
"simple, obvious and wrong".
Phages are intensely species specific to bacterial species, so they don't work unless you identify exactly what you're targeting. Also, even if they can penetrate biofilms, that doesn't mean you can successfully deliver them to the biofilm in the human body, since they have to survive the whole blood stream and the normal human immune response to "not self" things.
3 replies →
> you can't patent phages, so we'll just continue ignoring them
Nope. Plenty of governments fund this sort of research. And chances are there isn’t an off-the-shelf phage that ticks the boxes, which means you need some amount of genetic engineering, in which case Monsanto has your back.
This is a nicely-designed study. For decades, we've known that inflammation is a risk factor for heart attacks.
In this study, the researchers designed a custom antibody that binds to oral bacteria. Then they used histological staining to identify specific biofilm structures inside the atherosclerotic tissue. Bacteria released from the biofilm were observed in heart attack cases, which gives us evidence that when the body's immune system responded to these bacteria, it triggered inflammation which ruptured cholesterol-laden plaque. So now we have more insight into the mechanism behind why inflammation is associated with heart attack risk.
The "pantheon" of risk factors for heart disease are:
* hs-CRP (inflammation): the mechanism studied by this research. High inflammation roughly doubles your risk of heart disease.
* ApoB - 20% of people with normal cholesterol will have abnormal ApoB, and be at risk of heart disease (ApoB is a structural protein in lipoproteins which cause arterial plaque).
* Lp(a) - the strongest hereditary risk factor for heart disease (Lp(a) acts as a multiplier on ApoB, since it camouflages cholesterol particles from your liver)
* HbA1c - insulin resistance /diabetes is a risk factor for just about everything.
* eGFR - estimates the volume of liquid your kidneys can filter, and is an input to the latest heart disease risk models (PREVENT).
All of these risk factors can be measured with a blood test + doctor review. Easy to order online: https://www.empirical.health/product/comprehensive-health-pa...
You should probably disclose that the order link at the end of your post goes to your own company.
Basic LDL cholesterol and triglycerides blood panels are still an essential part of heart disease bloodwork, too.
I would suggest most people start by asking your doctor for some of these tests at your next annual checkup, as many of them and the doctor visit are likely covered by insurance. The ACA has special handling for routine annual checkups, so don’t assume it’s going to be expensive until you’ve checked the cost with your insurance. A routine bloodwork panel will also include a number of other important measures that are routine and very cheap. It’s helpful to have all of these on your medical record so trends can be identified over time.
Fwiw, since it seems like a number of people on here have Kaiser, my experience asking my Kaiser pcp for these as a mid-30s otherwise healthy person:
-lp(a) and apob were covered
-ldl is computed on the standard panel, not an actual measurement
-accidentally got lp(a) twice and it varied quite a bit, so they may use different labs that are calibrated differently
-hs-crp is not offered
-doctor didn’t seem particularly aware of the more “niche” tests but was open to putting them in during my yearly physical
Basic LDL cholesterol is often covered by insurance, but ApoB, Lp(a), and hs-CRP are unfortunately usually not. If insurance doesn't end up covering it, sometimes the fee is just ridiculous.
For example, one person got billed $1,338 for just an ApoB test when insurance denied coverage: https://www.reddit.com/r/PeterAttia/comments/14a4an1/apob_te...
Part of why we do cash pay (and pre-negotiated pricing with the labs) is that you avoid weird catastrophic scenarios like this. The price is upfront and transparent.
(It's too late to edit the original post, but my affiliation is on my HN profile.)
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IANAD, but
1) Isn't ApoB measurement pretty much in tandem with LDL, VLDL, and triglycerides? I realize it's being recognized now as the necessary factor for arterial dysfunction, but it seems like a lot of hoopla is being made as if it were some "silent" overlooked factor when for the vast, vast majority of people their ApoB levels are entirely explained by the other 3 lipid panel line items carrying it, and they have been in use for decades and are strongly targeted by the medical establishment
2) Isn't Lp(a) a separate lipoprotein altogether which is an independent risk factor for MACE? I've never heard of it "disguising" other cholesterol in testing.
1) ApoB itself is more accurate than LDL and triglycerides. The latest evidence is that ApoB and Lp(a) together are more accurate than even LDL, VLDL, non-HDL, triglerycerides, etc combined: https://academic.oup.com/eurheartj/article-abstract/46/27/27...
2) The terminology is confusing, but each Lp(a) particle is "just" a cholesterol particle wrapped with an extra protein, apoprotein (a). So each Lp(a) particle includes one ApoB molecule (the structural protein in atherogenic cholesterol particles) and many cholesterol and triglyceride molecules, but the extra protein makes each Lp(a) particle about 6x more atherogenic than a typical cholesterol particle.
you're correct
there's a small subset of people with more atherogenic triglycerides that ApoB picks up over and above just tracking with the LDL, but...you probably knew that just looking at them
The standard risk model based on SCORE-2 and PREVENT like parameters are very poor as reported in the recently published paper on the their accuracy performance by the Swedish team [1].
>All of these risk factors can be measured with a blood test + doctor review
As all CVD risk stratification with cardiologist review, the most important accuracy is sensivity (avoiding false negative that will escape review) of SCORE-2 and PREVENT, 48% and 26%, respectively [1].
The paper alternative proposal increased the sensitivity to 58% by performing clustering instead of conventional regression models as practiced in the standard SCORE-2 (Europe) and PREVENT (US).
These type of models including the latest proposal performed very poorly as indicated by their otherwise excellent and intuitive display of graphical abstract results [1].
[1] Risk stratification for cardiovascular disease: a comparative analysis of cluster analysis and traditional prediction models:
https://academic.oup.com/eurjpc/advance-article/doi/10.1093/...
Understanding this is a shameless plug, it's very cool this exists.
You don't need to use this specific blood test, by the way. Any lab near you will test these biomarkers for you.
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It being an ad casts suspicion on the entire post.
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What's the recommendation for someone with a hilariously high Lp(a)? Just pin LDL as low as possible?
Currently yes. There are some really promising drugs in the pipeline that are doing well in trials, though.
So is poor oral hygiene a risk factor?
It's been known for years that bad oral health leads to heart disease.
For lipids, besides the named tests, HDL, LDL, and triglyceride tests are older but shouldn't be overlooked.
For measuring inflammation, besides hs-CRP, additional tests are relevant and overlooked: regular CRP, ESR, and homocysteine.
Additionally, a heart attack can result from parasite induced inflammation too, e.g. in chagas disease, which is becoming increasingly common in the US while being very undetected without explicit testing. It is also very difficult to treat, but the gist 4196f31d12a43a95756e792500ff516f has some info on treating it. Lyme disease too can harm the heart permanently. In both cases a pacemaker could help as applicable.
Can you expand more on why you'd want regular CRP over hs-CRP (specifically for cardiovascular risk)?
For homocysteine, one proxy is B12 or folate (which are more cost-effective to test). To my knowledge, ESR is used in certain rheumatologic conditions, and was used more often in the past, but isn't currently used for heart disease.
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What do you do next if one is high? See your Doctor?
Yeah. If you don't have obvious symptoms, they'd likely prescribe you a statin, metformin, or some sort of dietary intervention. But you'd want to discuss it with your doctor in any case...
This particular panel includes a consult with a doctor (who can advise on next steps, prescribe medication, and so on). Or you can take the results to your doctor.
Is the fat rapture because the body wants fat to release vitamins and other stuff to help power itself to fight off the bacteria?
Do you happen to know how much that test costs? (Clicking a link to try to find out brought me to a page that asks for my zip code.)
> Do you happen to know how much that test costs?
FYI the person who posted the link is cofounder of the company he linked to.
You can ask your doctor to order these tests at your annual checkup, too.
That panel is $190.
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are you a cardiologist? Excellent points, thanks
Not a cardiologist, but adjacent to this type of research. I'm an MLE but have published research in cardiology.
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This has been suspected for decades.
https://www.thelancet.com/journals/laninf/article/PIIS147330...
Hopefully it leads somewhere that brings us new preventative care.
Might explain why some have success with carnivore. Less dental plaque.
The original title is "Myocardial infarction may be an infectious disease" which appears to be clickbait, with the title posted here being much more accurate.
Immune response to bacteria in arterial plaques can cause them to break up and cause the attack (my lay-interpretation) so the bacteria is a trigger, but "infectious disease" is a bit of hyperbole.
> bacteria in arterial plaques can cause them to break up and cause the attack
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix” whose rupture “result[s] in thrombus formation and ultimately myocardial infarction” sounds like infection more than careless bacteria kicking up muck.
Not all infarctions are due to infectious disease. The title (even on HN) is incorrect.
"Some myocardial infarctions attributed to an infectious disease."
"A myocardial infarction may be due to infectious disease."
My maternal grandfather died of an aortic separation. This caused a myocradial infarction, which was not due to infectious disease. I had my aortic valve replaced with a mechanical when I was 2, and 9, and 31, so I'll have a more nuanced kind of heart failure.
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Have always been fascinated with Paul Ewald's arguments (as laid out in his books The New Germ Theory of Disease and Evolution of Infectious Disease) that most chronic illnesses are due to pathogens.
"The most unique finding in our study was that viridans streptococci seemed to colonize the lipid core and wall of an atheroma as a biofilm and that this biofilm was not recognized by cells of the innate immune system. "
This is a pretty cool finding. Biofilms are also beyond reach of antibacterials usually. And seing a commensal become a problem due to "location, location, location" is also cool.
Nice article. Cool leads
This raises two questions.
- Does this suggest that courses of antibiotics might reduce heart attack risk?
- Does this suggest that regular use of, e.g., Listerine might reduce heart attack risk? (While, perhaps, slightly increasing esophageal cancer risk.)
It would be interesting to run an epidemiological study to see if current interventions move the needle in a meaningful way.
Listerine would make it worse for sure.
Don't use "antiseptic" mouthwash; it kills beneficial bacteria in the mouth, causing bad bacteria to multiply.
I have personal experience of this.
agreed, after much research the only mouth wash i use is therasol
For the Listerine part: they are referencing this study: https://pubmed.ncbi.nlm.nih.gov/16373688/ that seems to show a correlation between poor oral health and sudden cardiac death, so it might help indeed, with other good oral health practices.
I only use very dilute Listerine - for the fluoride. A dentist told me that undiluted, alcohol based products can cause tissue damage (which conceivably would result in a vector for oral bacteria infiltrating to the bloodstream?)
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I probably should find sources first but I was always under the impression that the mouth biome is strongly correlated to gut biome which strongly correlated to immune system.
TFA says the biofilms protect the bacteria from antibiotics. Better approach is probably engineered antibodies or even a phage (engineered virus that attacks the bacteria).
Yes, there are studies where they compared heart attack rates for people who'd taken a course of antibiotics with those who hadn't and there was quite a large effect in some of them.
eg. https://www.science.org/content/article/antibiotics-cut-hear...
Titles like this are very confusing. The paper better explains it, but a disease can't be contagious or infectious. The paper describes a link between a potential bacterial infection and myocardial infarctions that may take years or decades to develop.
The disease is only the named group of symptoms. The potential cause of the disease is the bacterial infection. Those are very different concepts.
Wild I see only one mention of COVID so far, it has been shown to attack all kinds of organ tissues, the perspectives around "with or from" somehow permanently prevents people from discussing the underlying changes from this continued global cycling of the pathogen.
There are already pretty serious blood disorders linked directly to oral health (https://en.wikipedia.org/wiki/Actinomycosis almost took down slackware linux)
I think I'll go floss.
yeah and dehydration is not good, saliva flow is protective
This seems like a good explanation of how my father died. He had the flu, and died overnight from a massive heart attack.
https://www.health.harvard.edu/heart-health/what-does-the-fl...
How does flu affect the heart? The virus only rarely infects the heart directly. Instead, the adverse effects of the virus on the heart are due to atherosclerosis of the arteries of the heart. Many people over age 50 have atherosclerosis — and in some people it has not yet been diagnosed. Because atherosclerosis narrows the arteries and reduces the flow of blood, less oxygen reaches the heart muscle. When the effect of the flu on the lungs lowers the amount of oxygen in the blood, this further reduces the supply of oxygen to the heart. This can lead to a heart attack or cardiac arrest (sudden death).
Is this risk more than theoretical? Many careful studies have shown there is an increased risk of heart disease following a bout of flu. In one study of 80,000 adults with influenza, nearly 12% had a serious cardiac event, such as a heart attack, during or in the weeks after getting the flu.
> In one study of 80,000 adults with influenza, nearly 12% had a serious cardiac event, such as a heart attack, during or in the weeks after getting the flu.
That sounds really high
Okay I just looked it up and this was only among hospitalized individuals which makes a lot more sense because most people just stay home unless it's very bad but that is still surprising to me
For sure it exacerbated an existing cardiovascular system. Once the system is weakened things cause big problems quickly.
In the context of the article, it's inflammation rupturing the 'fibrous cap' on plaque deposits leading to a heart attack, so I presume OP is talking about the inflammatory response to having the flu.
> How does flu affect the heart?
Even temporary stress on the respiratory system can cause long-term damage to the brain, lungs, and heart. Because of Covid, we started to learn that an acute, severe infection can affect people much later.
That research led to the beginning of an understanding that repeated flu infections can contribute to premature death even many decades later.
sure does. chain of events. The epidemiologists should be able to validate these claims.
The bacterial contribution to MACE has been an ongoing subject of investigation for decades
https://www.nejm.org/doi/full/10.1056/NEJMoa043526
still hasn't really panned out
This has been known for at least 5 years though, but good to see this topic resurface
Wasn't that a plot in DBZ where a virus weakens Goku's heart?
https://dragonball.fandom.com/wiki/Heart_Virus Indeed!
see https://pubmed.ncbi.nlm.nih.gov/17420199/
It's been known for many years that the flu vaccine reduces heart attack incidence. The flu either causes lasting damage to the cardiovascular system or directly causes heart attacks.
This is perfectly well known and absolutely nothing new.
This study merely expands research on the topic (focus on bacteria+biofilm instead of flu).
So "Myocardial infarction may be an infectious disease" is a weird clickbait title. We know. We knew for a long time.
We also have quite a few of anti biofilm agents in IV formulations that could have an effect inside of the cardiovascular system if used in high dosages, but the molecules are old, cheap and unsexy, so no one will try. (ambroxol and NAC come to mind)
Great concept..
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Typical of the medical field: one of the most studied diseases in the past several decades and now there is a ground-breaking new study that questions all knowledge. I blame the corruption from American medical experts and organizations which only object is to sell drugs.
This does not question all knowledge. Bacteremia and cardiac disease have been linked for years (see upvoted comment above), which is why these studies were done in the first place. This study isn't ground breaking, it's extending an already established area of study.
Furthermore, while there are issues of misaligned incentives across the industry, of the top 10 pharma companies: Roche, AstraZeneca, Bayer, Novartis, Sanofi, Novo Nordisk, GSK, are all based in Europe, so your assertion further down makes no sense.
In what sense does it “question all knowledge”?
This idea is not supported by the study in question. Even if it were, what you’re describing is just how science works! The cynicism, while understandable, seems widely irrelevant here.
How science works in America perhaps. Not in Europe. Your "conclusion" about the study is ludicrous, please read it again.